The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
A dysbiotic microbiome triggers T H 17 cells to mediate oral mucosal immunopathology in mice and humans
Open accessAbstract
Combined patient and animal model studies implicate microbiota-triggered T H 17 cells as disease drivers and therapeutic targets in periodontitis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Studies using germ‐free mice have also been employed in the context of the oral microbiome, demonstrating the role of diabetes in disrupting the equilibrium of the oral microbiota50 and confirming the role of the oral microbiota in periodontal disease pathogenesis.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“In line with the role of oral mucosa as a physiological barrier, the functions of immune networks within this mucosa reflect the site‐specific challenges faced within the oral cavity. For example, they contribute to homeostasis in response to masticatory forces and trigger immune responses to the development of pathologic microbial communities.52, 53”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“Microbial dysbiosis is also necessary for additional inflammatory responses characteristic of periodontal disease, including local expansion of pathologic interleukin‐17+/CD4+ T‐helper (T‐helper 17) cells.52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“The importance of commensal species to pathogenesis is further demonstrated by the requirement for commensal microbial communities in the instigation of disease by periodontal pathogens.51, 52”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
In the citing paper
“homeostatic T‐helper 17 cells were found to be induced by mechanical stimuli in a microbiome‐independent manner, whereas periodontitis‐associated T‐helper 17 cells were found to accumulate in a microbiome‐dependent manner and to require both interleukin‐6 and interleukin‐23.”
From The oral microbiome: Role of key organisms and complex networks in oral health and disease (2021) · cites this paper as [52]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria
Ivanov, I. I., Atarashi, K., Manel, N., Brodie, E. L., Shima, T., Karaoz, U., Wei, D., Goldfarb, K. C., Santee, C. A., Lynch, S. V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.09.033 · Cited by 4,554 · cited 1×
“Microbial induction of TH17 cells has been well documented at various other barrier sites, including the lower GI (32) and skin (33).”
Periodontitis: from microbial immune subversion to systemic inflammation
Hajishengallis, G. (2015) · Nature Reviews Immunology · doi:10.1038/nri3785 · Cited by 3,046 · cited 2×
“To date, the pathogenic drivers of exaggerated destructive inflammation are incompletely understood, and treatment largely aims at reduction of microbial stimulation rather than at targeting of specific immune pathways through hostmodulation therapies (2).”
Self-citationPeriodontitis: a polymicrobial disruption of host homeostasis
Darveau, R. P. (2010) · Nature Reviews Microbiology · doi:10.1038/nrmicro2337 · Cited by 1,688
The IL-23-IL-17 immune axis: from mechanisms to therapeutic testing
Gaffen, S. L., Jain, R., Garg, A. V., & Cua, D. J. (2014) · Nature reviews. Immunology · doi:10.1038/nri3707 · Cited by 1,585
Update on Prevalence of Periodontitis in Adults in the United States: NHANES 2009 – 2012
Eke, P., Dye, B., Wei, L., Slade, G., Thornton-Evans, G., Borgnakke, W., Taylor, G., Page, R., Beck, J., & Genco, R. (2015) · The Journal of Periodontology · doi:10.1902/jop.2015.140520 · Cited by 1,442
Targeting IL-17 and TH17 cells in chronic inflammation
Miossec, P., & Kolls, J. K. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3794 · Cited by 1,414
Homeostatic Immunity and the Microbiota
Belkaid, Y., & Harrison, O. J. (2017) · Immunity · doi:10.1016/j.immuni.2017.04.008 · Cited by 1,261 · cited 1×
“DISCUSSION At mucosal barrier sites, the local immune system is tasked with the delicate act of maintaining a dynamic balance between host and environmental stimuli (26).”
Self-citationSTAT3 Mutations in the Hyper-IgE Syndrome
Holland, S. M., DeLeo, F. R., Elloumi, H. Z., Hsu, A. P., Uzel, G., Brodsky, N. N., Freeman, A. F., Demidowich, A. P., Davis, J., Turner, M. L. C., et al. (2007) · New England Journal of Medicine · doi:10.1056/nejmoa073687 · Cited by 1,233
Self-citationInduction and molecular signature of pathogenic TH17 cells
Lee, Y., Awasthi, A., Yosef, N., Quintana, F. J., Xiao, S., Peters, A., Wu, C., Kleinewietfeld, M., Kunder, S., Hafler, D. A., et al. (2012) · Nature Immunology · doi:10.1038/ni.2416 · Cited by 1,174 · cited 2×
“In human lesions of periodontitis, we document an expansion of TH17 cells that secrete cytokines associated with pathogenic activity (10, 30) and are predominantly resident memory TH17 cells (31).”
Impaired TH17 cell differentiation in subjects with autosomal dominant hyper-IgE syndrome
Milner, J. D., Brenchley, J. M., Laurence, A., Freeman, A. F., Hill, B. J., Elias, K. M., Kanno, Y., Spalding, C., Elloumi, H. Z., Paulson, M. L., et al. (2008) · Nature · doi:10.1038/nature06764 · Cited by 1,157
Self-citationAbusleme, L., Dupuy, A. K., Dutzan, N., Silva, N., Burleson, J. A., Strausbaugh, L. D., Gamonal, J. A., & Diaz, P. I. (2013) · The ISME Journal · doi:10.1038/ismej.2012.174 · Cited by 1,118 · cited 2×
“Standardof-care treatment of periodontal disease currently aims at removal of the periodontitis-associated microbial commensal communities (37, 41, 42) by means of mechanical dental debridement with adjunct systemic antibiotics for severe disease (43).”
Self-citationCompartmentalized Control of Skin Immunity by Resident Commensals
Naik, S., Bouladoux, N., Wilhelm, C., Molloy, M. J., Salcedo, R., Kastenmuller, W., Deming, C., Quinones, M., Koo, L., Conlan, S., et al. (2012) · Science · doi:10.1126/science.1225152 · Cited by 1,092
Self-citationChronic Mucocutaneous Candidiasis in Humans with Inborn Errors of Interleukin-17 Immunity
Puel, A., Cypowyj, S., Bustamante, J., Wright, J. F., Liu, L., Lim, H. K., Migaud, M., Israel, L., Chrabieh, M., Audry, M., et al. (2011) · Science · doi:10.1126/science.1200439 · Cited by 1,056 · cited 1×
“Specifically, patients with primary immunodeficiencies affecting either TH17 cell differentiation or function (12, 13) all have susceptibility to oral candidiasis.”
Griffen, A. L., Beall, C. J., Campbell, J. H., Firestone, N. D., Kumar, P., Yang, Z. K., Podar, M., & Leys, E. J. (2011) · The ISME Journal · doi:10.1038/ismej.2011.191 · Cited by 1,006
Distribution and compartmentalization of human circulating and tissue-resident memory T cell subsets
Sathaliyawala, T., Kubota, M., Yudanin, N., Turner, D., Camp, P., Thome, J. J. C., Bickham, K. L., Lerner, H., Goldstein, M., Sykes, M., et al. (2013) · Immunity · doi:10.1016/j.immuni.2012.09.020 · Cited by 848
IL-17 Signaling: The Yin and the Yang
Amatya, N., Garg, A. V., & Gaffen, S. L. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.01.006 · Cited by 785
Interleukin-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability
Lee, J. S., Tato, C. M., Joyce-Shaikh, B., Gulen, M. F., Cayatte, C., Chen, Y., Blumenschein, W. M., Judo, M., Ayanoglu, G., McClanahan, T. K., et al. (2015) · Immunity · doi:10.1016/j.immuni.2015.09.003 · Cited by 760
Diverse Targets of the Transcription Factor STAT3 Contribute to T Cell Pathogenicity and Homeostasis
Durant, L. R., Watford, W. T., Ramos, H. L., Laurence, A. D. J., Vahedi, G., Wei, L., Takahashi, H., Sun, H., Kanno, Y., Powrie, F. M., et al. (2010) · Immunity · doi:10.1016/j.immuni.2010.05.003 · Cited by 751
Neutrophils as protagonists and targets in chronic inflammation
Soehnlein, O., Steffens, S., Hidalgo, A., & Weber, C. (2017) · Nature reviews. Immunology · doi:10.1038/nri.2017.10 · Cited by 623 · cited 1×
“Although it is well established that neutrophils secrete tissue-destructive proteases (53), further work is needed to dissect mechanisms by which neutrophils mediate downstream osteoclast activation and bone loss.”
BackgroundPolymicrobial synergy and dysbiosis in inflammatory disease
Lamont, R. J., & Hajishengallis, G. (2015) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2014.11.004 · Cited by 585
Self-citationOptimization of the ligature-induced periodontitis model in mice
Abe, T., & Hajishengallis, G. (2013) · Journal of Immunological Methods · doi:10.1016/j.jim.2013.05.002 · Cited by 550 · cited 1×
“11 of 12 For experimental periodontitis studies in mice, LIP was performed as previously described (18) in different strains of mice in the presence or absence of ATB treatments, RORt inhibition, FTY720 treatment, or antibody treatments to block IL-17, Ly6G, or isotype controls.”
Self-citationFocused specificity of intestinal TH17 cells towards commensal bacterial antigens
Yang, Y., Torchinsky, M. B., Gobert, M., Xiong, H., Xu, M., Linehan, J. L., Alonzo, F., Ng, C., Chen, A., Lin, X., et al. (2014) · Nature · doi:10.1038/nature13279 · Cited by 520
Basic biology and role of interleukin‐17 in immunity and inflammation
Zenobia, C., & Hajishengallis, G. (2015) · Periodontology 2000 · doi:10.1111/prd.12083 · Cited by 503 · cited 1×
“In our current work, we focused on the TH17 cell subset, which is not only pivotal for oral antifungal immunity (11, 25) but also has been documented to expand in the oral inflammatory disease, periodontitis (6, 28, 29).”
Self-citationInterleukin 17 is a chief orchestrator of immunity
Veldhoen, M. (2017) · Nature Immunology · doi:10.1038/ni.3742 · Cited by 490 · cited 1×
“IL-1 and IL-23 have also been linked to TH17 differentiation and/or expansion in other settings (9).”
The leukocyte integrin antagonist Del-1 inhibits IL-17-mediated inflammatory bone loss
Eskan, M. A., Jotwani, R., Abe, T., Chmelar, J., Lim, J.-H., Liang, S., Ciero, P. A., Krauss, J. L., Li, F., Rauner, M., et al. (2012) · Nature Immunology · doi:10.1038/ni.2260 · Cited by 429
Self-citationThe dichotomous nature of T helper 17 cells
Stockinger, B., & Omenetti, S. (2017) · Nature reviews. Immunology · doi:10.1038/nri.2017.50 · Cited by 419
Tissue-Specific Immunity at the Oral Mucosal Barrier
Moutsopoulos, N. M., & Konkel, J. E. (2017) · Trends in Immunology · doi:10.1016/j.it.2017.08.005 · Cited by 415 · cited 1×
“It is the initial portal of encounter for microbes, food, and airborne antigens as they enter the GI tract, all in the context of mechanical stress (mastication) (27).”
Self-citationDiabetes Enhances IL-17 Expression and Alters the Oral Microbiome to Increase Its Pathogenicity
Xiao, E., Mattos, M., Vieira, G. H. A., Chen, S., Corrêa, J. D., Wu, Y., Albiero, M. L., Bittinger, K., & Graves, D. T. (2017) · Cell Host & Microbe · doi:10.1016/j.chom.2017.06.014 · Cited by 396 · cited 1×
“IL-17 has previously been shown to be a primary mediator of periodontal immunopathology in settings of altered background immunity such as immune deficiency (54, 55), diabetes (56), and aging (57).”
Host defense against oral microbiota by bone-damaging T cells
Tsukasaki, M., Komatsu, N., Nagashima, K., Nitta, T., Pluemsakunthai, W., Shukunami, C., Iwakura, Y., Nakashima, T., Okamoto, K., & Takayanagi, H. (2018) · Nature Communications · doi:10.1038/s41467-018-03147-6 · Cited by 330
Moutsopoulos, N. M., Konkel, J. E., Sarmadi, M., Eskan, M. A., Greenwell‐Wild, T., Dutzan, N., Abusleme, L., Zenobia, C., Hosur, K. B., Abe, T., et al. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3007696 · Cited by 310 · cited 1×
“IL-17 has previously been shown to be a primary mediator of periodontal immunopathology in settings of altered background immunity such as immune deficiency (54, 55), diabetes (56), and aging (57).”
Self-citationCharacterization of the human immune cell network at the gingival barrier
Dutzan, N., Konkel, J. E., Greenwell-Wild, T., & Moutsopoulos, N. M. (2016) · Mucosal Immunology · doi:10.1038/mi.2015.136 · Cited by 305
Self-citationLoss of STAT3 in CD4+ T Cells Prevents Development of Experimental Autoimmune Diseases
Liu, X., Lee, Y. S., Yu, C., & Egwuagu, C. E. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.9.6070 · Cited by 289
Xiao, S., Yosef, N., Yang, J., Wang, Y., Zhou, L., Zhu, C. Y., Wu, C., Baloglu, E., Schmidt, D. R., Ramesh, R., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.04.004 · Cited by 283 · cited 1×
“Similarly, in our pharmacological inhibition of RORt, we selected a small-molecule inhibitor (GSK805) that preferentially targets TH17 cell differentiation (45) while sparing other sources of IL-17 (22).”
Hajishengallis, G., & Lamont, R. J. (2016) · Trends in Microbiology · doi:10.1016/j.tim.2016.02.010 · Cited by 275
Self-citationEvidence of the presence of T helper type 17 cells in chronic lesions of human periodontal disease
Cardoso, C. R. D. B., Garlet, G. P., Crippa, G. E., Rosa, A. L., Júnior, W. M., Rossi, M. A., & Silva, J. S. (2008) · Oral Microbiology and Immunology · doi:10.1111/j.1399-302x.2008.00463.x · Cited by 270
Kantarcı, A., Oyaizu, K., & Dyke, T. E. V. (2003) · Journal of Periodontology · doi:10.1902/jop.2003.74.1.66 · Cited by 269
Dutzan, N., Abusleme, L., Bridgeman, H., Greenwell-Wild, T., Zangerle-Murray, T., Fife, M. E., Bouladoux, N., Linley, H., Brenchley, L., Wemyss, K., et al. (2017) · Immunity · doi:10.1016/j.immuni.2016.12.010 · Cited by 252
Self-citationWithers, D. R., Hepworth, M. R., Wang, X., Mackley, E. C., Halford, E. E., Dutton, E. E., Marriott, C. L., Brucklacher-Waldert, V., Veldhoen, M., Kelsen, J. R., et al. (2016) · Nature Medicine · doi:10.1038/nm.4046 · Cited by 245
Identification of Natural RORγ Ligands that Regulate the Development of Lymphoid Cells
Santori, F. R., Huang, P., van de Pavert, S. A., Douglass, E. F., Leaver, D. J., Haubrich, B. A., Keber, R., Lorbek, G., Konijn, T., Rosales, B. N., et al. (2015) · Cell Metabolism · doi:10.1016/j.cmet.2015.01.004 · Cited by 238 · cited 1×
“These inhibitors may be ideally suited for localized diseases, such as periodontitis, where local treatment can avoid systemic effects on thymocyte and lymph node development (47, 49).”
Verma, A. H., Richardson, J. P., Zhou, C., Coleman, B. M., Moyes, D. L., Ho, J., Huppler, A. R., Ramani, K., McGeachy, M. J., Mufazalov, I. A., et al. (2017) · Science Immunology · doi:10.1126/sciimmunol.aam8834 · Cited by 219 · cited 1×
“Innate, antigenindependent TCR+IL-17+ cells have also been shown to expand at the oral barrier (specifically within the tongue) in response to Candida infection (35) and could conceivably be a contributing source of TCR+IL-17+ in periodontitis.”
BackgroundPosition Paper: Systemic Antibiotics in Periodontics
Slots, J. (2004) · Journal of Periodontology · doi:10.1902/jop.2004.75.11.1553 · Cited by 215
Porphyromonas gingivalis promotes Th17 inducing pathways in chronic periodontitis
Moutsopoulos, N. M., Kling, H. M., Angelov, N., Jin, W., Palmer, R. J., Jr., Nares, S., Osorio, M., & Wahl, S. M. (2012) · Journal of Autoimmunity · doi:10.1016/j.jaut.2012.03.003 · Cited by 212 · cited 1×
“1D), suggesting a bias toward TH17 cell differentiation in disease lesions (16, 17).”
Self-citationGlowacki, A. J., Yoshizawa, S., Jhunjhunwala, S., Vieira, A. E., Garlet, G. P., Sfeir, C. S., & Little, S. R. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1302829110 · Cited by 205
IL ‐17: overview and role in oral immunity and microbiome
Abusleme, L., & Moutsopoulos, N. M. (2016) · Oral Diseases · doi:10.1111/odi.12598 · Cited by 189
Self-citationThe Involvement of IL-23 and the Th17 Pathway in Periodontitis
Ohyama, H., Kato‐Kogoe, N., Kuhara, A., Nishimura, F., Nakasho, K., Yamanegi, K., Yamada, N., Hata, M., Yamane, J., & Terada, N. (2009) · Journal of Dental Research · doi:10.1177/0022034509339889 · Cited by 184
Neutrophil Hyper-responsiveness in Periodontitis
Matthews, J. B., Wright, H. J., Roberts, A., Ling‐Mountford, N., Cooper, P. R., & Chapple, I. (2007) · Journal of Dental Research · doi:10.1177/154405910708600806 · Cited by 183 · cited 1×
“Neutrophil accumulation is also known as a hallmark of human periodontitis and has been long speculated as a driver of pathology (23, 51, 52).”
Interleukin-12 and Interleukin-23 Blockade in Leukocyte Adhesion Deficiency Type 1
Moutsopoulos, N. M., Zerbe, C. S., Greenwell‐Wild, T., Dutzan, N., Brenchley, L., DiPasquale, G., Uzel, G., Axelrod, K. C., Lisco, A., Notarangelo, L. D., et al. (2017) · New England Journal of Medicine · doi:10.1056/nejmoa1612197 · Cited by 176 · cited 2×
“We have identified IL-23/IL-17 dysregulation in periodontitis associated with the rare genetic disorder, leukocyte adhesion deficiency type 1 (LAD1), and have exploited that target by IL-23 blockade in humans (55).”
BackgroundSelf-citationSmall molecule inhibitors of ROR γt: Targeting T h17 cells and other applications
Huh, J. R., & Littman, D. R. (2012) · European Journal of Immunology · doi:10.1002/eji.201242740 · Cited by 174
Subgingival Microbiome Shifts and Community Dynamics in Periodontal Diseases
Diaz, P. I., Hoare, A., & Hong, B. (2016) · Journal of the California Dental Association · doi:10.1080/19424396.2016.12221035 · Cited by 152
Self-citationImmune and regulatory functions of neutrophils in inflammatory bone loss
Hajishengallis, G., Moutsopoulos, N. M., Hajishengallis, E., & Chavakis, T. (2016) · Seminars in Immunology · doi:10.1016/j.smim.2016.02.002 · Cited by 150
Self-citationAl‐Mossawi, H., Chen, L., Fang, H., Ridley, A., de Wit, J., Yager, N., Hammitzsch, A., Pulyakhina, I., Fairfax, B. P., Simone, D., et al. (2017) · Nature Communications · doi:10.1038/s41467-017-01771-2 · Cited by 142
Position Paper Periodontal Maintenance
Cohen, R. E. (2003) · Journal of Periodontology · doi:10.1902/jop.2003.74.9.1395 · Cited by 127
Comprehensive Periodontal Therapy: A Statement by the American Academy of Periodontology
(2011) · Journal of Periodontology · doi:10.1902/jop.2011.117001 · Cited by 101 · cited 2×
“10 of 12 Although the link of commensal microbes to periodontal destructive inflammation is well documented clinically (42), the mechanisms by which commensal bacteria induce pathogenic inflammation in periodontitis are poorly understood.”
Allam, J., Duan, Y., Heinemann, F., Winter, J., Götz, W., Deschner, J., Wenghoefer, M., Bieber, T. R. M., Jepsen, S. V., & Novak, N. (2011) · Journal Of Clinical Periodontology · doi:10.1111/j.1600-051x.2011.01752.x · Cited by 94
Mendelian Genetics of Human Susceptibility to Fungal InfectionPreprint
Lionakis, M. S., Netea, M. G., & Holland, S. M. (2014) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a019638 · Cited by 88
Self-citationInhibition of RORγT Skews TCRα Gene Rearrangement and Limits T Cell Repertoire Diversity
Guo, Y., MacIsaac, K. D., Chen, Y., Miller, R. J., JAIN, R. K., Joyce-Shaikh, B., Ferguson, H. M., Wang, I., Cristescu, R., Mudgett, J. S., et al. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.11.073 · Cited by 58 · cited 1×
“These inhibitors may be ideally suited for localized diseases, such as periodontitis, where local treatment can avoid systemic effects on thymocyte and lymph node development (47, 49).”
Oral Microbiome Characterization in Murine Models
Abusleme, L., Hong, B.-Y., Hoare, A., Konkel, J. E., Diaz, P., & Moutsopoulos, N. (2017) · BIO-PROTOCOL · doi:10.21769/bioprotoc.2655 · Cited by 58
Self-citationNares, S., Moutsopoulos, N. M., Angelov, N., Rangel, Z. G., Munson, P. J., Sinha, N., & Wahl, S. M. (2009) · American Journal Of Pathology · doi:10.2353/ajpath.2009.080677 · Cited by 36 · cited 1×
“1D), suggesting a bias toward TH17 cell differentiation in disease lesions (16, 17).”
Self-citation
Flagged first, then by citations
Cited by
Sorted by citations
Local and systemic mechanisms linking periodontal disease and inflammatory comorbidities
Hajishengallis, G., & Chavakis, T. (2021) · Nature Reviews Immunology · doi:10.1038/s41577-020-00488-6 · Cited by 1,871
Self-citationOsteoimmunology: evolving concepts in bone–immune interactions in health and disease
Tsukasaki, M., & Takayanagi, H. (2019) · Nature reviews. Immunology · doi:10.1038/s41577-019-0178-8 · Cited by 812
The oral microbiome: Role of key organisms and complex networks in oral health and disease
Sedghi, L., DiMassa, V., Harrington, A., Lynch, S. V., & Kapila, Y. L. (2021) · Periodontology 2000 · doi:10.1111/prd.12393 · Cited by 755
The role of the microbiota in periodontal disease
Curtis, M. A., Diaz, P. I., & Van Dyke, T. E. (2020) · Periodontology 2000 · doi:10.1111/prd.12296 · Cited by 698
Self-citationThe cytokine network involved in the host immune response to periodontitis
Pan, W., Wang, Q., & Chen, Q. (2019) · International Journal of Oral Science · doi:10.1038/s41368-019-0064-z · Cited by 740
Metadata
- Authors
- Dutzan, N., Kajikawa, T., Abusleme, L., Greenwell-Wild, T., Zuazo, C. E., Ikeuchi, T., Brenchley, L., Abe, T., Hurabielle, C., Martin, D., Morell, R. J., Freeman, A. F., Lazarevic, V., Trinchieri, G., Diaz, P. I., Holland, S. M., Belkaid, Y., Hajishengallis, G., & Moutsopoulos, N. M.
- Affiliations
- Oral Immunity and Inflammation Unit, NIDCR, NIH, Bethesda, MD 20892, USA.
- University of Pennsylvania (US)
- National Institutes of Health (US)
- Genomics and Computational Biology Core, NIDCD, NIH, Bethesda, MD 20892, USA.
- UConn Health (US)
- Corresponding author
- Moutsopoulos, Niki M.
- ORCID
- Dutzan, Nicolas
- Kajikawa, Tetsuhiro
- Abusleme, Loreto
- Zuazo, Carlos E.
- Ikeuchi, Tomoko
- Brenchley, Laurie
- Abe, Toshiharu
- Hurabielle, Charlotte
- Martin, Daniel
- Morell, Robert J.
- Freeman, Alexandra F.
- Lazarevic, Vanja
- Trinchieri, Giorgio
- Diaz, Patricia I.
- Holland, Steven M.
- Belkaid, Yasmine
- Hajishengallis, George
- Moutsopoulos, Niki M.
- Venue
- Science Translational Medicine
- Published
- 2018-10-17
- Volume
- 10
- Issue
- 463
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC6330016
- OpenAlex
- W2896857921
- Cited by
- 382
- References
- 58
- Citations by year
- 2026: 38 · 2025: 46 · 2024: 49 · 2023: 46 · 2022: 47 · 2021: 70 · 2020: 57 · 2019: 28 · 2018: 1
- FWCI
- 44.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondation pour la Recherche Médicale
- NIAID (IRP)
- NIDCR (Intramural, DE024153, DE026152)
- NCI Intramural
- La Roche-Posay
- CEDEF
- Philippe Foundation
- fondation groupe pasteur mutualité
- Société Française de Dermatologie
- Topics
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- dysbiosis, oral microbiota, Th17 cells, oral inflammation, periodontitis, oral immunity, targeted therapy
- MeSH terms
- Animals, Bacteria, Bone Resorption, Cell Differentiation, Humans, Inflammation, Mouth Mucosa, Neutrophils, Periodontitis, Interleukin-6, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Microbiota, Dysbiosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
